In acute Phencyclidine toxicity there are four “C’s”: combativeness, catatonia, convulsions and coma. These effects are dose-related. Combativeness and catatonia are frequently observed together at the lower dosages, while convulsions and coma are related to higher dosage effects. During this stage, one also sees hypertensive crisis sufficiently severe to be fatal, although such crises are relatively rare in our experience. Illusions can dominate: space walking, the detachment of sounds, objects changing in size, shape, and distance. Visual illusions rather than true hallucinations are common, but occasionally auditory hallucinations occur. If the dose of Phencyclidine is high enough, the patient may have many grand mal seizures and coma which require hospitalization and supportive care to stabilize and maintain the respiratory and cardiovascular function. With proper management, most patients who go into a PCP-induced coma survive, although the period of coma may be quite prolonged. Our experience indicates that the usual duration of acute Phencyclidine toxicity is 0 to 72 hours. Lab results indicate that blood is almost always positive and urine is positive. A large number of people clear after stage I, Phencyclidine acute toxicity; some go into stage II, Phencyclidine toxic psychosis.

Acute Phencyclidine Toxicity: Case 1

At a rock concert in the San Francisco Bay Area, six adolescents who had previously experimented with a variety of psychoactive drugs, including PCP, ingested an unknown quantity of Phencyclidine in tablet form. Although they had experience with PCP, they had been primarily smoking it in a form of “krystal joints,” and this was their first exposure to the tablet form of PCP. All six became acutely intoxicated; one, a 17-year-old white male high school senior, became comatose. Friends took him to the emergency room of a local hospital after observing the young man for a couple of hours and becoming concerned over his extreme muscular rigidity and shallow respirations. He was hospitalized and maintained on a respirator for over three days. With this supportive management he recovered fully, but there was a period of cerebral dysfunction with poor memory and depression lasting for over a week following the acute Phencyclidine toxicity. This case example also demonstrates that a patient can go from stage I acute Phencyclidine toxicity to stage IV, cerebral dysfunction and depression, without going through stage II and stage III psychotic phases.

Acute Phencyclidine Toxicity: Treatment of Stage I

Acute Phencyclidine toxicity patients can be divided into two groups: those who are comatose, and those who are acutely intoxicated but conscious.

A. Comatose Patients

As in the management of any coma patient, the first level of consideration is stabilization of the ventilation and cardiovascular systems, and protecting the individual from inflicting bodily harm. Secondly, consideration should be given to the elimination of the offending agent.

Respiratory depression with pure Phencyclidine is unusual except in very high dosages. However, respiratory depression may be marked when combined with alcohol, other sedative hypnotics, or opiates. If the patient is sufficiently depressed, respiratory assistance on a respirator is necessary.

B. Conscious Patients

Patients in acute toxicity may also present as psychiatric emergencies with symptoms of paranoia, agitation, thought disorder, negativism, hostility, and grossly altered body image. Assaultive and antisocial behavior often results in the individual’s coming to the attention of treatment personnel. In the management of such individuals, Luisada and Brown (1976) have delineated the immediate goals of treatment as: 1) prevention of injury to the patient or others; 2) assurance of continuing treatment; 3) reduction of stimuli; 4) amelioration of the psychosis: and 5) the reduction of agitation. The reduction of external stimulation through the use of seclusion or a “quiet room” is of prime importance. Clinicians disagree as to the most appropriate pharmacological intervention. Luisada and Brown (1976) recommend chlorpromazine (Thorazine), although we generally prefer diazepam (Valium) for symptomatic or behavioral control. Haloperidol (Haldol) has also been used ().

C. Elimination of Phencyclidine from the body

Although many clinicians prefer conservative supportive management, Aronow, Miceli, and Done (this volume) have successfully utilized continuous gastric suction, acidification of the urine, and a potent diuretic such as furosemide (Lasix) to enhance elimination of the PCP. Their technique and rationale for use are described in detail in other papers in this volume. Phencyclidine is recycled through the enterohepatic circulation, and introducing a slurry of activated charcoal into the intestine may decrease reabsorption of Phencyclidine from the small intestine. This should not be used instead of gastric suction in a comatose patient; however, 100 ml of activated charcoal slurry should be inserted into the stomach just before the nasogastric tube is removed, or may be given orally to a non-comatose patient.

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